ArticleThe Journal of physiology2010
Flufenamic acid decreases neuronal excitability through modulation of voltage-gated sodium channel gating.
Article in The Journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 60 citations in OpenAlex.
- A Systemically Administered Humanized Anti-Nav1.7 Antibody with Long-Lasting Analgesic Activity and Preserved Physiological Nociception.Pharmaceutics · 2026Article
- Plasma KCC2, NKCC1, and GABA as peripheral biomarkers in autism spectrum disorder: a combined ROC analysis.Metabolic brain disease · 2026Article
- Nonsteroidal Anti-Inflammatory Drugs as Modulators of Cation Channels: Fenamates Repurposing in Channelopathies.ChemMedChem · 2025Review
- Extinction of contextual fear memory is facilitated in TRPM2 knockout mice.Molecular brain · 2025Article
- Anesthetic- and Analgesic-Related Drugs Modulating Both Voltage-Gated NaBiomolecules · 2024Review
- Antiseizure properties of fenamate NSAIDs determined in mature human stem-cell derived neuroglial circuits.Frontiers in pharmacology · 2024Article
- Review
- Fenamates Inhibit Human Sodium Channel Nav1.2 and Protect Glutamate-Induced Injury in SH-SY5Y Cells.Cellular and molecular neurobiology · 2020Article
- Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants-Possible Involvement in Pain Alleviation.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Involvement of TRPC4 and 5 Channels in Persistent Firing in Hippocampal CA1 Pyramidal Cells.Cells · 2020Article
- Critical Components for Spontaneous Activity and Rhythm Generation in Spinal Cord Circuits in Culture.Frontiers in cellular neuroscience · 2020Article
- Article
- Differential Contribution of CaFrontiers in cellular neuroscience · 2017Article
- A novel computational biostatistics approach implies impaired dephosphorylation of growth factor receptors as associated with severity of autism.Translational psychiatry · 2014Article
- Rhythmic bursting in the pre-Bötzinger complex: mechanisms and models.Progress in brain research · 2014Article
- Do canonical transient receptor potential channels mediate cholinergic excitation of cortical pyramidal neurons?Neuroreport · 2013Article
- Flufenamic acid as an ion channel modulator.Pharmacology & therapeutics · 2013Review
- Slowly inactivating component of Na+ current in peri-somatic region of hippocampal CA1 pyramidal neurons.Journal of neurophysiology · 2013Article
- Sodium and calcium mechanisms of rhythmic bursting in excitatory neural networks of the pre-Bötzinger complex: a computational modelling study.The European journal of neuroscience · 2013Article
- Pretreatment with nonselective cationic channel inhibitors blunts the PACAP-induced increase in guinea pig cardiac neuron excitability.Journal of molecular neuroscience : MN · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The electrophysiological phenotype of individual neurons critically depends on the biophysical properties of the voltage-gated channels they express. Differences in sodium channel gating are instrumental in determining the different firing phenotypes of pyramidal cells and interneurons; moreover, sodium channel modulation represents an important mechanism of action for many widely used CNS drugs. Flufenamic acid (FFA) is a non-steroidal anti-inflammatory drug that has been long used as a blocker of calcium-dependent cationic conductances. Here we show that FFA inhibits voltage-gated sodium currents in hippocampal pyramidal neurons; this effect is dose-dependent with IC(50) = 189 μm. We used whole-cell and nucleated patch recordings to investigate the mechanisms of FFA modulation of TTX-sensitive voltage-gated sodium current. Our data show that flufenamic acid slows down the inactivation process of the sodium current, while shifting the inactivation curve ~10 mV toward more hyperpolarized potentials. The recovery from inactivation is also affected in a voltage-dependent way, resulting in slower recovery at hyperpolarized potentials. Recordings from acute slices demonstrate that FFA reduces repetitive- and abolishes burst-firing in CA1 pyramidal neurons. A computational model based on our data was employed to better understand the mechanisms of FFA action. Simulation data support the idea that FFA acts via a novel mechanism by reducing the voltage dependence of the sodium channel fast inactivation rates. These effects of FFA suggest that it may be an effective anti-epileptic drug.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.